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*
British Heart Foundation Cardiovascular Medicine Unit, National Heart and Lung Institute, Imperial College School of Medicine, Hammersmith Hospital, London, United Kingdom; and
Celltech Ltd., Slough, United Kingdom
4 Abbreviations used in this paper: EC, endothelial cells; Pt, platelets; CS, contact sensitivity; ID, injected dose; i.d., intradermal; OX, 4-ethoxymethyl-2-phenyl-2-oxazolin-5-one (oxazolone).
The selectins are adhesion molecules that mediate the tethering and
rolling of leukocytes on vascular endothelium. Although E-selectin and
P-selectin are known to be expressed by endothelial cells (EC) in
response to proinflammatory stimuli, their pattern and mechanisms of
expression in immune-mediated inflammation remain poorly understood. By
quantifying luminal endothelial selectin expression via i.v.
administration of radiolabeled mAb, we detected constitutive expression
of P-selectin, but not E-selectin, in mouse skin. Both selectins were
transiently up-regulated after intradermal TNF-
, IL-1
, or
IL-1ß. In contrast, during a contact sensitivity response to
oxazolone, expression of both selectins was prolonged, with distinct
peaks at 6 and 48 h. Experiments with P-selectin gene-targeted
mice showed that the P-selectin measured was exclusively expressed by
EC rather than platelets. The early and late phases of selectin
expression in contact sensitivity were differentiated in terms of their
requirement for prior sensitization, and the action of IL-1. Whereas
the early phase was a nonspecific irritant response to oxazolone,
the late phase was Ag specific and was partially IL-1 dependent.
Therefore, persistence of both E- and P-selectin expression in vivo can
occur as a result of sequential and distinct EC activation processes
that appear to be at least partially different from those previously
reported as stimulating ICAM-1 and VCAM-1 expression. The further
elucidation of mechanisms of EC activation in this model may help
determine the relative roles of selectins and ligands for leukocyte
integrins in the sequential recruitment of T cells and other leukocyte
subsets during ongoing immune-mediated inflammatory
responses.
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